Differential regulation of atrial contraction by P1 and P2 purinoceptors in normotensive and spontaneously hypertensive rats
| Autor: | Juliano Quintella Dantas Rodrigues, Kleber de Magalhães Galvão, Aron Jurkiewicz, Regiane Miranda-Ferreira, Antonio G. García, Afonso Caricati-Neto, Edilson Dantas da Silva, Neide H. Jurkiewicz |
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| Rok vydání: | 2013 |
| Předmět: |
Inotrope
medicine.medical_specialty Carbonyl Cyanide m-Chlorophenyl Hydrazone Contraction (grammar) Nifedipine Physiology Uridine Triphosphate Neurotransmission Adenosine Triphosphate Internal medicine Rats Inbred SHR Internal Medicine medicine Purinergic P2 Receptor Antagonists Animals cardiovascular diseases Heart Atria Rats Wistar Atrium (architecture) Dose-Response Relationship Drug Ryanodine receptor Chemistry Receptors Purinergic P2 Ryanodine Purinergic receptor Antagonist Receptors Purinergic P1 musculoskeletal system Calcium Channel Blockers Myocardial Contraction Electric Stimulation Mitochondria Rats Endocrinology Purinergic P1 Receptor Antagonists Hypertension cardiovascular system Calcium Cardiology and Cardiovascular Medicine medicine.drug |
| Zdroj: | Hypertension research : official journal of the Japanese Society of Hypertension. 37(3) |
| ISSN: | 1348-4214 |
| Popis: | In the normotensive rat atrium, adenosine-5'-triphosphate and uridine-5'-triphosphate exert a biphasic effect consisting of an initial negative inotropic effect (NIE) followed by a subsequent positive inotropic effect (PIE). We comparatively studied these responses in normotensive Wistar rats (NWRs) and spontaneously hypertensive rats (SHRs). Compared with NWRs, the NIE responses in the atria were lower and the PIE responses were higher in SHRs. The P1 purinoceptor antagonist, D 8-cyclopentyl-1,3-dipropylxanthine, partially blocked the NIE responses of both ATP and UTP and mildly enhanced the PIE responses in both NWRs and SHRs. Furthermore, the P2 purinoceptor blockers suramin and pyridoxalphosphate-6-azophenyl-2',4'-disulphonic acid tetrasodium salt induced a pronounced block of the PIE responses in both atria types. The PIE responses to ATP were inhibited more efficiently by nifedipine. These responses were depressed by ryanodine and, to a lesser extent, carbonyl cyanide 3-chlorophenylhydrazone in SHR atria compared with NWR atria. The higher responses in SHR rats suggest the existence of an augmented endoplasmic reticulum Ca(2+) store and faster mitochondrial Ca(2+) cycling in SHR atria compared with NWR atria. These data support the hypothesis that a dysfunction of purinergic neurotransmission and enhanced sympathetic activity are contributing factors in the pathogenesis of hypertension. |
| Databáze: | OpenAIRE |
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